Persistent, isolated pulmonary vein re-entry: inducibility, entrainment, and overdrive termination of a sustained tachycardia within an isolated pulmonary vein

Abstract

Pulmonary veins (PVs) are the predominant sources of paroxysmal atrial fibrillation (AF), and electrical PV isolation has become an established interventional treatment for patients suffering from AF. There are a few cases describing PV tachycardias; however, mechanisms of PV arrhythmogenicity resulting in PV tachycardias remain incompletely understood. We report on a patient who underwent PV isolation for paroxysmal AF, in whom a persistent PV tachycardia was observed within an isolated vein. This tachycardia was stable in nature and different pacing manoeuvres revealed electrophysiological features consistent with reentry (Lasso displaying the entire tachycardia cycle length, concealed entrainment, overdrive termination, and induction by programmed stimulation) as the underlying mechanism.

Introduction

As the pulmonary veins (PVs) became the main target for catheter ablation of atrial fibrillation (AF), ¹ many studies have been performed to elucidate the mechanisms of PV arrhythmogenicity. Experimental and clinical data demonstrated distinctive anatomical and electrophysiological properties of the PV musculature and the PV ostial region with a complex muscle fibre orientation, short refractory periods, and decremental conduction properties. These characteristics create a substrate for re-entry and therefore it is one of the presumed mechanisms of PV arrhythmogenicity. ² However, there are only a few cases demonstrating electrophysiological characteristics favouring re-entry in PV tachycardias. ^{3 , 4}

We report a patient with paroxysmal AF undergoing PV isolation who demonstrated a persistent tachycardia within an isolated PV with features consistent with re-entry as the underlying mechanism.

Case report

A 44-year-old man was referred for PV isolation because of recurrent symptomatic and drug refractory episodes of paroxysmal AF. The left atrial diameter was slightly enlarged (42 mm) and left ventricular function was normal.

The first procedure was started during sinus rhythm. The electrophysiological study was performed in a fasting state and under mild sedation. The following catheters were introduced via the femoral veins: (i) a steerable quadripolar catheter (Xtrem, ELA Medical, Le-Plessis-Robinson, France) was positioned in the coronary sinus; (ii) a decapolar circumferential mapping catheter (Lasso ^TM , Biosense Webster Inc., Diamond Bar, CA, USA) was used for PV mapping; and (iii) ablation was performed using a 3.5 mm externally irrigated-tip catheter (Celsius ThermoCool ^TM , Biosense-Webster Inc.). After transseptal puncture, a single bolus of 50 IU/kg heparin was administered and the activated clotting time was kept above 250 s throughout the procedure. Despite high-rate atrial burst pacing up to a minimal cycle length (CL) before reaching local refractoriness, all induced AF episodes persisted for <1 min. Thus, PV isolation was performed during sinus rhythm. After successful electrical isolation of all four PVs and cavo-tricuspid isthmus ablation with the achievement of bidirectional block, rapid atrial burst pacing again failed to induce sustained AF.

Two days after the initial ablation, a second procedure was performed because of recurrent atrial tachycardia (AT), with a regular atrial CL of 240 ms. The mapping of the PVs, performed during ongoing AT, was started at the left PVs that demonstrated recovered electrical conduction. Accordingly, these veins were targeted for re-isolation and the patient converted to sinus rhythm during RF delivery at the ostium of the left inferior PV (LIPV), revealing PV tachycardia from the left veins as the underlying mechanism of the AT. After isolation of the LIPV, mapping of the left superior PV (LSPV) now also demonstrated complete block, indicating simultaneous isolation of both left veins by closing the conduction gap at the LIPV.

Further mapping of the right veins demonstrated complete isolation of the right inferior PV. However, a persistent regular tachycardia with a CL of 220 ms was observed within the right superior PV (RSPV), although the patient still remained in sinus rhythm ( Figure  1 ), indicating complete electrical isolation of the RSPV. The Lasso catheter displayed a significant part of the tachycardia CL (180 ms), suggesting a possible re-entrant mechanism. The tachycardia terminated reproducibly by incremental overdrive pacing and was re-induced by programmed stimulation. Pacing at a CL of 200 ms through the Lasso catheter demonstrated concealed entrainment with an appropriate post-pacing interval ( Figure  2 ). Additionally, programmed stimulation within the isolated RSPV revealed an ultra-short effective refractory period (ERP) of 70 ms ( Figure  3 ). After a waiting period of 45 min, a persistent isolation of all four PVs was confirmed by the demonstration of entrance and exit blocks.

Discussion

In the present case, a stable sustained tachycardia was observed within an electrically isolated PV, demonstrating all features required for re-entry as the underlying mechanism: the tachycardia was inducible by programmed stimulation, amenable for entrainment with a fixed post-pacing interval, and terminated by overdrive pacing, respectively. Furthermore, almost the entire tachycardia CL could be displayed in the circumferential PV mapping catheter.

Previous publications reporting on the mapping of PV tachycardias emphasize the difficulty to demonstrate clear evidence for the tachycardia mechanism. Mapping and mechanistic proof of PV tachycardias challenge electrophysiologists due to short tachycardia CL, the potentially unstable nature of the tachycardia, and the difficulty to pace with consistent capture within an isolated PV. ⁵ Takahashi et al.³ were able to induce sustained PV tachycardias in <3% of the patients after PV isolation, of which some demonstrated features consistent with re-entry. However, the assumed mechanism of re-entry was challenged because of fusion of activation during entrainment pacing at a CL <180 ms, rather than representing significant parts of the tachycardia CL and the lack of programmed stimulation to demonstrate decremental conduction, respectively. In the presented case, programmed stimulation revealed decremental conduction properties with an extremely short ERP within the isolated PV. Additionally, the sustained PV tachycardia had a relatively slow CL (220 ms) and entrainment pacing showed >80% of the CL without fusion of activation.

Furthermore, PV tachycardia mapping in humans is limited due to the restricted resolution of currently available mapping tools to display the propagation of excitation within the PV. Recently, two in part simultaneously running PV tachycardias have been described in an isolated left superior PV, which were explored by a 20-polar multi-spine catheter. ⁶ Interestingly, these tachycardias demonstrated electrophysiological characteristics consistent with a focal mechanism underlying both, triggered activity and enhanced automaticity. In two other studies, PV tachycardias have been investigated using a multi-electrode basket catheter, the tool with the highest mapping density available thus far. Kumagai et al.² performed programmed stimulation within the PV and induced a short-lived reentrant circuit with the exit and entrance at the PV–LA junction that starts AF. In contrast, in a study by Arentz et al. , ⁷ PV basket mapping revealed that arrhythmogenic activity during AF induction is predominantly caused by focal activity. However, in these studies, mapping was performed before isolation of the veins, and the electrical interaction between the veins and the atria with induction of AF and subsequent intermittent passive activation of the vein prevented a stable setting of the PV tachycardia. Hence, no pacing manoeuvre within the PV could be performed, e.g. to demonstrate concealed entrainment.

In an experimental study, Arora et al.⁸ performed high-resolution optical mapping of the PVs and the PV–LA junction in an isolated, coronary-perfused canine model. The authors induced non-sustained consecutive beats by programmed stimulation and visualized the complete excitation within a circuit, indicating a re-entrant mechanism. Thus, distinct anatomical and electrophysiological PV properties as well as data derived from experimental and clinical observations suggest that re-entry is a potential mechanism at least in a subset of PV tachycardias. However, as all PV mapping tools so far available for a percutaneous electrophysiological procedure in humans are limited by the extent of resolution, the definitive proof of the underlying mechanism(s) is still lacking. Mapping tools as available for experimental studies are desired to overcome current limitations of human PV mapping to finally reveal the actual underlying mechanism of (sustained) human PV tachycardias by visualizing the exact excitation propagation. Although often challenging in the clinical setting, in the presented case, all conventional techniques could be applied to investigate the underlying mechanism of the observed tachycardia and all features consistent with re-entry have been demonstrated, thus adding another piece to the puzzle of PV tachycardia mechanisms.

References